The effects of atherosclerotic epicardial stenosis on coronary vascular resistance can be understood in terms of basic fluid mechanical principles. Resistance is directly related to the trans-stenotic pressure drop and inversely related to flow. However, even with a fixed anatomic stenosis, resistance is not fixed; it increases as trans-stenotic flow increases. This exacerbates the pressure drop across the stenosis that develops as a result of flow; at high flows, large pressure drops can occur. This characteristic of flow through stenotic lesions can contribute to a "steal" physiology, between either epicardial or intramural coronary arteries. Studies have also shown the clinical importance and influence of dynamic alterations in coronary resistance, occurring either at the large or small vessel level. In addition, compressive forces exerted by the myocardium or by elevated intraventricular pressures can increase coronary vascular resistance, and therefore can interfere with myocaridal perfusion. All these factors must be considered in order to understand the mechanisms leading to myocardial ischemia, and therefore to the clinical syndrome of angina pectoris. Further studies have shown the complex interaction of the coronary vessles and to peripherical vascular bed. The vessels of each group were treated as resistance vessels either in series or in parallel configuration. The results have demonstrated dramatically the individual and collective contribution of these vessels towards the maintenance if sufficient myocardial perfusion.